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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1989-9-20
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pubmed:abstractText |
We reported that TSH and insulin-like growth factor-I (IGF-I), which were known to synergistically stimulate DNA synthesis, synergize to elevate the 1,2-diacylglycerol content of FRTL-5 thyroid cells. We presented evidence that cAMP is the proximal mediator of these actions of TSH. To further define the mechanism of this interaction, we investigated the effects of IGF-I on TSH stimulation of adenylyl cyclase. Long and short term effects of IGF-I or high doses of insulin were studied in FRTL-5 cells that were maintained in serum-, hormone-, and growth factor-free medium for 4-7 days (basal cells). When cells were incubated with high doses of insulin for 7 days and acutely stimulated, a 10-fold increase in sensitivity and a 2-fold increase in maximal responsiveness of cAMP accumulation to TSH were observed. To study shorter term effects, cells were preincubated with insulin for 3 h and then exposed to TSH, cholera toxin, or forskolin. Incubation with high doses of insulin for 3 h caused 30-300% increases in cAMP accumulation at high doses of TSH (greater than or equal to 1 mU/ml), cholera toxin (greater than 0.1 microM), and forskolin, but did not affect the EC50 for TSH. Dose-response studies were consistent with insulin acting via receptors for IGF-I, and IGF-I caused a similar effect. There was a 45% increase in adenylyl cyclase activity stimulated by TSH in membranes isolated from cells incubated with high doses of insulin for 3 h. Pretreatment of FRTL-5 cells with pertussis toxin, which ADP-ribosylates the inhibitory G-protein Gi, or adenosine, which we show inhibits cAMP accumulation by interacting with Gi, did not affect insulin/IGF-I enhancement of cAMP accumulation. We suggest that synergism of actions of TSH and IGF-I may in part be due to IGF-I enhancement of TSH stimulation of adenylyl cyclase.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/Adenylate Cyclase Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Forskolin,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/Pertussis Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Somatomedins,
http://linkedlifedata.com/resource/pubmed/chemical/Thyrotropin,
http://linkedlifedata.com/resource/pubmed/chemical/Virulence Factors, Bordetella
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0013-7227
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
125
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1315-20
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:2547582-Adenylate Cyclase,
pubmed-meshheading:2547582-Adenylate Cyclase Toxin,
pubmed-meshheading:2547582-Animals,
pubmed-meshheading:2547582-Cell Line,
pubmed-meshheading:2547582-Cyclic AMP,
pubmed-meshheading:2547582-Forskolin,
pubmed-meshheading:2547582-Insulin,
pubmed-meshheading:2547582-Insulin-Like Growth Factor I,
pubmed-meshheading:2547582-Kinetics,
pubmed-meshheading:2547582-Pertussis Toxin,
pubmed-meshheading:2547582-Somatomedins,
pubmed-meshheading:2547582-Thyroid Gland,
pubmed-meshheading:2547582-Thyrotropin,
pubmed-meshheading:2547582-Virulence Factors, Bordetella
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pubmed:year |
1989
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pubmed:articleTitle |
Insulin-like growth factor-I potentiates thyrotropin stimulation of adenylyl cyclase in FRTL-5 cells.
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pubmed:affiliation |
Department of Medicine, Cornell University Medical College, New York, New York 10021.
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pubmed:publicationType |
Journal Article
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